Hypothalamic Control of Eating Flashcards
Why do we stop eating?
Satiety
What signals satiety in the short term?
CCIC released in the GI tract!
-Signal sent to brainstem via vagus nerve
What signals satiety in the long term?
Fat releases Leptin. This signals to the hypothalamus.
the combined short and long term signals in the brainstem and hypothalamus cause:
-Stop eating & Dec. food intake!
What controls meal size?
“Satiety” signals
What short-term signals cause decreased eating?
- Oropharyngeal
- Gastric distention vs. gastric nutrient satiety
- Post-absorptive Satiety
What is the oropharyngeal short term signal?
Putting food in mouth/taste:
- Fed state: dec. feeding
- Fasting state: inc. feeding
What was the Phillips and Powley gastric infusion mouse study?
Made mice they could deliver food directly too using pyloric cuff between the stomach and intestines.
What did they find in the gastric infusion study?
- Gastric stretch –> causes decreased food intake
- Gastric nutrients (putting sucrose into the stomach) —> caused no further decrease in food intake
(nutrient value had no effect, just stretch) - Intestinal nutrients –> Sucrose in the intestines caused —-> decreased food intake
What factors cause pre absorptive satiety?
- Gastric stretch
2. Intestine nutrients (calories)
What causes post-absorptive satiety?
Liver factors! The portal vein has sensors: 1. Glucose 2. Free fatty acids [These both decrease food intake]
How does gastric distention cause changes in the CNS that cause decreased food intake?
- Causes increased mechanoreceptor activity
- These mechanoreceptors cause Inc. in Vagus activity
- This information is sent from vagus nerve to NTS (Nucleus Tractus Solitarius - Solitary Nucleus)
- The NTS causes decreased food intake
What does leptin do to gastric stretch?
Increases responsiveness to gastric stretch/more sensitivity (it takes less food to cause decreased food intake) - Leptin is in the brainstem acting on vagal afferents and solitary (NTS) tract.
What releases CCK (Cholecystokinin) and why?
Duodenum, in response to meals
What does CCK act on and what does this pathway cause?
It acts on CCK receptors –> inc. stimulation of vagal afferents —> Inc. stimulation in NTS —> Dec. food intake
What does CCK (Cholecystokinin) cause in the body?
- Inc. gallbladder contraction –> releases bile for fat digestion
- Inc. pyloric constriction –> inc. stomach activity –> promotes digestion
- Inc. gastric contractions –> inc. stomach activity –> promotes digestion
What releases Gherkin and what does it cause?
Released from stomach
- > It’s increased by fasting
- > Orexigenic effect: Inc. appetite
What is Prader-Willi syndrome & what are its symptoms?
Deletion on chromosome 15, 1/25,000 Symptoms: -Fetal hypotonia (dec. muscle tone) -Mental retardation -Hypogonadotropic hypogonadism (Dec. FSH, Dec. LH --> Dec. gonado function) -Obesity -Hyperphagia (excessive eating)
What hormone is high in Prader-Willi?
High blood Ghrelin, which increases appetite
What releases Leptin? What type of signal is it?
Adipocytes, its a long-term satiety signal
fat stores are controlled by “adiposity” signals
What might overweight people have a problem with?
Leptin receptors!
What is Leptin?
- Ob protein/gene product
- Adipocytes release leptin and it causes Dec. food intake
Where does leptin work?
- Brainstem (NTS)
2. Hypothalamus
What is the role of ghrelin again?
Inc. food intake!
Where does ghrelin act?
Inc. NPY neuronal activity within ARC (Arcuate nucleus)
Where is the LHA (Lateral Hypothalamic Area)?
On the lateral areas/wings of coronal section
What happens when you lesion the LHA (lateral hypothalamic area)?
Don’t eat/cessation of eating (Aphagia)
What causes aphagia in LHA damage?
- Damage to the medial forebrain bundle (part of mess-limbic system) that causes (1) reduced motivation to eat and (2) reduced motor function (axons damaged may be involved in motor control)
- Loss of neurons that synthesize “orexigenic” peptide
What happens when LHA is stimulated?
Release of “anabolic” neurotransmitted in the brainstem
—> causes increased eating!
What happens when the PVN is activated/stimulated?
Activation of PVN –> release of “catabolic - break down” (dec. eating) neurotransmitters in brainstem
What does the paraventricular nucleus (PVN) cause?
Releases oxytocin & vasopressin from same neurons.
PVN neurons send axons to brainstem to regulate food intake —> Dec. eating
What does the ARC (arcuate nucleus) do? What does it have?
It integrates information.
It has two populations of neurons:
1. Neuropeptide Y (NPY)
2. Melanocortin (POMC-derived peptide)
Where do Neuropeptide Y (NPY) and Melanocortin (POMC-derived peptide) project?
PVN and LHA nuclei!
What does Neuropeptide Y (NPY) neurons cause?
Inc. eating (through projections to PVN & LHA)
What does Melanocortin (POMC-derived peptide) cause?
Dec. eating (through projections to PVN & LHA)
What does Leptin inhibit in the ARC? What does it cause?
It inhibits NPY neurons, causing decreased food intake.
What does Leptin activate in the ARC? What does it cause?
It activates melanocortin activity, causing decreased food intake
What does NPY do overall?
Inc. Eating
What does Alpha-MSH do overall?
Melanocortin: Dec. eating
What does Leptin do overall?
Dec. eating
What does CRH do overall?
Dec. eating
What does Orexin do overall?
Inc. eating
What does CCK do overall?
Dec. eating/motor movement
What does Gastric stretch do overall?
Dec. eating/motor movement
